Supplementary Material for: Host Genetics, Steatosis and Insulin Resistance among African Americans and Caucasian Americans with Hepatitis C Virus Genotype-1 Infection
2009-04-25T00:00:00Z (GMT) by
Hepatic steatosis is the accumulation of fat in liver cells. Insulin resistance (IR) occurs when normal amounts of insulin do not stimulate insulin activity in cells. Both conditions have been described in hepatitis C virus (HCV) infection and are thought to be biologically related. This study examined the association of genetic variants with steatosis and IR among 167 African Americans and 184 Caucasian Americans with HCV genotype-1. Steatosis was defined as at least 5% of fat in cells on liver biopsy. IR was quantified as a score greater than 2 from the Homeostasis Model Assessment, version 2.2 (HOMA2-IR). Associations were investigated by estimating odds ratios separately by race. Statistically significant associations (p < 0.05) were observed for variants in <i>interleukin-10 (IL10)</i>, <i>leptin receptor (LEPR)</i>, <i>interleukin-6 (IL6)</i> and <i>transforming growth factor beta-1 (TGF-</i>β<i>1)</i> for both outcomes. Some significant interactions were observed between <i>IL10,</i><i>LEPR </i>and <i>TGF-</i>β<i>1 </i>polymorphisms and HOMA2-IR scores when examining steatosis. The interaction of HOMA2-IR and <i>IL10</i> was consistent in both races whereas for <i>LEPR</i> and <i>TGF-</i>β<i>1</i> the interactions were statistically significant in only one of the racial groups.These results could imply that some <i>IL10,</i><i>LEPR </i>and <i>TGF-</i>β<i>1 </i>polymorphisms may modify an association between steatosis and IR.